The purpose of the Brain Today blog is to distill the daily news about brain health and help the public understand the essential meaning of each article. Through time however, I have found myself clarifying the same themes over and over again. Five of these themes are explored in this five-part series “How to Read the News About Alzheimer’s and Dementia”.

How to Read the News About Alzheimer’s and Dementia - Part 1 Be Aware of the Author’s Definition of Alzheimer’s Disease

A major source of unintended confusion about Alzheimer’s disease (AD) is the inconsistent definition of this disease from one article to the next. In many instances, the author uses a definition that the reader might not fully understand. I explored this problem more fully in an earlier post (When Does Alzheimer’s Disease Really Begin?) but I will summarize it succinctly here.
The problem is that research scientists think about the disease in terms of pathology and speak about it in those terms. Given the long underlying process of amyloid accumulation in the brain, they contend that AD begins decades prior to the first clinical symptoms of memory loss.

Physicians, on the other hand, use a strict clinical definition of the disease stating that AD begins when the underlying pathology (amyloid accumulation) has caused enough brain damage to render the patient demented. In this scenario, the disease begins many years after the first clinical symptoms.

Most lay-people default to a symptom-based understanding and consider the disease present when the symptoms first appear. This occurs at some mid-point between the other two perspectives.

When you read the news, it is important to understand the potential for confusion in this regard. Here are a few of the many examples of how confusion arises:

If an article says that a drug is useful in treating early-stage AD, you should be careful to understand what the author means by “early-stage”. They might mean "30 years prior to symptoms" or they might mean "the point at which the patient becomes demented". Unfortunately, such claims often breed false hope and are usually not meaningful to those recently diagnosed with AD because, by all definitions, we rarely diagnose the disease early.

When you read that AD is difficult to distinguish from normal aging, be aware that this is true for some definitions of AD but not for others. There is certainly a clear distinction from normal aging once clinical symptoms appear.

When you read about mild cognitive impairment (MCI) and that it may or may not convert to AD, don’t be accidentally misled. Focus on any information indicating the cause of the MCI. If it is AD pathology, then scientists would agree that the patient already has the disease while physicians would argue against an AD diagnosis until the symptoms progress to dementia.

Keep in mind these multiple definitions for AD that are commonly used in the press and it will help you to avoid misleading conclusions about otherwise clear news items.

Here are the links to each other part of this series:Part 2 of 5: Don't be Mislead by Data on Treatment EfficacyPart 3 of 5: Common Assertions about Diagnostic Accuracy Hide TruthPart 4 of 5: The Term "Dementia" Cannot be Interpreted LooselyPart 5 of 5: "No Cure" Not as Bad as it Sounds

In my self appointed role as "clarifier of the news" in the brain health space, I find that, on occasion, it is a very easy job. For instance, today.

This summary justification from the BBC, making the case for increasing public funds that support Alzheimer's research is eloquent, accurate, and important. I don't feel compelled to add a thing other than my hearty recommendation that you follow the link and read it.

Contributed by: Dennis Fortier, President, Medical Care Corporation________________________________________________If you look for news about brain health, you have no doubt seen lots of coverage this week of a study published in the Journal of Agricultural and Food Chemistry suggesting great cognitive benefits from drinking wild blueberry juice.

There are solid theoretical grounds to support this finding but it may be a little early to celebrate the end of dementia. While I always root for these studies to be confirmed through more rigorous methods, I will keep my expectations low on this one for the following reasons.

First of all, many studies have been initiated on the theoretical groundwork that foods rich in anti-oxidants might foster brain health and could confer improved cognitive capabilities. To date, none of these studies has been verified positive in that regard.

Secondly, this latest study was very small with only 18 research subjects enrolled; nine of whom drank blueberry juice and nine of whom were given a placebo drink.

And finally, the results are reported in a slightly misleading way. The statistically significantly improvement on two tasks (paired associate learning and list recall) was derived by comparing an initial score for each subject to their scores after 12 weeks of "therapy" (consuming either blueberry juice or a placebo drink believed to be blueberry juice). While both groups improved over the 12 weeks, there was not a significant difference between the group who got the blueberry juice and the group who got placebo. In this regard, we may find that all of the "gains" reported in this small test were due to the placebo effect.

Each year, about 700,000 people in the USA suffer a stroke. While it is certainly true that stroke can be deadly, it is the third leading cause of death behind heart disease and cancer, it can also cause significant cognitive changes in those who survive.

These changes may be subtle and cause mild cognitive impairment or they may be more severe resulting in dementia. Following are 7 interesting facts to help you better understand the impact of stroke.

1. While stroke is the third leading cause of death, it is the second most common cause of cognitive impairment and dementia.

2. Even damage to a small portion of the brain can have serious consequences. In fact, a thimble full of damaged brain due to stroke can cause dementia.

3. Stroke begins after age 50 and can gradually build up in the brain for decades. This gradual accumulation of tiny strokes can interfere progressively with the brain’s function until the individual becomes demented.

4. The risk of developing cognitive impairment is highest in those persons with vascular risk factors. These factors include:

High Blood Pressure or Low Blood Pressure

High Cholesterol

Obesity

Diabetes

Atherosclerosis (hardening of the arteries)

Minimal physical exercise (less than 2 days/week and 30 mins/session)

Smoking

Alcohol dependence

Prior stroke.

5. The most common types of cognitive problems due to are disturbances of attention, language, memory and executive function.Executive function is the ability to analyze, interpret, plan, organize, and execute complex instructions.

6. The risk of cognitive impairment and dementia, as well as the rate of cognitive decline in cerebrovascular disease, is highly correlated with underlying risk factors for stroke.

7. If left untreated, vascular cognitive impairment and dementia worsen. Annual screening for cognitive impairment in attention, memory and executive function starting at age 50 will help detect gradually accumulating cerebrovascular disease that may otherwise typically be undetected for many years.

A good additional source of information about risks for dementia is PreventAD.com. The site is sponsored by Medical Care Corporation but, like this blog, it is non-commercial and seeks only to educate. This content about stroke was a popular article from a past issue of Ounce of Prevention, the newsletter associated with that site.

The evidence has been accumulating for years, from a variety of sources, on multiple aspects of cognition and brain health, that physical exercise is great for your brain. While the specific mechanisms driving the health benefits are not well understood, the relationship is clear.

An excellent summary of the evidence was published today the blog BrainandSpinalCord.org. Among the facts are several indications that physical exercise may be a boon to recovery and healing of injuries. Additionally there is evidence that it can be neuro-protective and play a role in certain debilitating neurologic disorders such as Parkinson's disease and Alzheimer's disease.

The Washington Post has a health related blog (The Checkup) that often presents interesting viewpoints on a variety of topics. I like reading it and generally find the information useful. Today was not one of those days.

In today's post, the authors argue that it may be better not to know if one is genetically predisposed to higher risk for Alzheimer's disease. As regular readers of this blog already know, that represents a poor understanding of the facts and a position that, for most people, is not in the best interest of health.

Below is the body of the comment I left at "The Checkup".

At the risk of offending the author, it should be noted that "not wanting to know if one is genetically predisposed to Alzheimer's disease" is not a very defensible position once inspected under an educated light.

First, having certain genetic variants (APOe4 or TOM40) may increase risk of one day developing Alzheimer's disease while having a certain others (CTEP) may decrease it. However, no combination of these genes approaches a certainty of fate, they merely suggest probabilities. To imply that learning a bit about one's genetics is akin to knowing the future is to overstate our current understanding of genetics and Alzheimer's disease.

Second, like the author suggested with regards to breast cancer, there is plenty one can do to reduce risks for Alzheimer's (more so than one can do to reduce the risks for breast cancer). For example, there is solid scientific evidence that we should all maintaining good cardio-vascular health (lower LDL's, obesity and BP), enjoy a brain healthy diet (green leafy vegetables, berries, fish with Omega-3's, and fewer fats), remain intellectually and physically active, and stay socially engaged. A few other well supported life-style decisions would be to protect the head against the potential of injury and to stop smoking and excessive drinking. All good advice but perhaps more compelling if one knows they have a high genetic risk for a dementing disorder such as Alzheimer's.

Third, because early stage Alzheimer's has symptoms that look exactly like normal, age-related cognitive decline, it often goes undiagnosed and untreated during its earliest and most treatable stages. If one knows there is an increased genetic risk for the disease, it is more likely that early symptoms will be more vigilantly investigated and medical intervention might occur in a more timely and efficacious manner.

Finally, as other commenters have noted, the problem should be considered in a context broad enough to include more than just the patient. Many other lives are often affected and proper planning can be beneficial to all. The problem of Alzheimer's disease is greatly exacerbated by late detection; a phenomenon that is perpetrated by the antiquated "better not to know" dogma. That may have been true 20 years ago but we need to embrace a higher level of understanding. Journalists who continue to promote that idea are on the wrong side of the solution.

According to a recent publication in Cell Death and Disease, there is a credible link and a real possibility that, in the future, we will examine the health of cells on the retina as a gauge to determine the presence and/or progression of brain disease.

A good summary of the research, conducted at University College London, was published by the BBC today. The approach, tried only in mice to date, is to use florescent dye that binds to dead cells as a means of visually assessing the overall health of cells on the retina. To the extent that the health of the retina is correlated with the health of the brain, this could have intriguing possibilities.

It seems like we are often on a quest to identify those genes associated with disease and/or other attributes of poor health and function. However, a well sustained, albeit less publicized, parallel effort is underway to identify genes associated with good health. Researchers from the Albert Einstein College of Medicine have now published in the Journal of the American Medical Association their findings on such a gene.

According to their research, having two copies of a particular CETP variant was highly associated with slower memory decline and general brain health. While this gene variant has long been known to have an association with longevity and with good vascular health, it has never been definitively associated with brain health.

This study confirms what many had hypothesized and represents good news for those with this genetic profile.

One unanswered question, which may be the topic of further study, is how this relates to previous knowledge about the increased risks for Alzheimer's conferred by the APOe4 gene? If both are present (APOe4 and CETP), how does that affect an individual's risk?

The news wires are abuzz with the findings of a new study published in Alzheimers' & Dementia. The study showed that some people with Alzheimer's disease who drank a mixture of three key nutrients for 12 weeks were more likely to show an improvement in short term memory than patients who drank a placebo substitute.

The buzz is driven by two forces.

One is the euphoric prospect that three nutrients (uridine, choline, and omega-3 fatty acids), all of which are found in human breast milk, might in some way help to treat Alzheimer's disease. This is certainly worthy of some fan fare. The other is the swift and negative reaction of academic experts whenever a for-profit venture makes health related claims about interventions that have not yet been fully validated by the scientific process.

In this case, it is too early to know if a meaningful discovery is at hand. The initial science looks promising and has good face validity but the effect of the drink was quite minimal and the scope of the study was small. I don't think it is fair for the scientific community to undermine this approach merely because there is a profit motive behind the science but that is a valid reason for tempering public expectations and for requiring solid, third-party validation of the initial approach.

According to a study recently published in the Journal of Alzheimer's Disease, healthy mice as well as mice with a form of Alzheimer's disease, showed cognitive benefits after long-term exposure to cell-phone levels of radiation. This is precisely the type of study that lends itself to misleading headlines.

The answer to the question "Can cell phones prevent Alzheimer's disease" is probably "no" but, in fairness, nobody really knows. The only study available on the topic was well done and was published in a high-quality journal after passing through a rigorous review process by other scientists with expertise in this area. That study suggests that the answer could be "yes".

So why would I say the answer is probably "no"? For the same reasons that the authors of the study might say so. Because there is no theoretical grounding for the finding, because the study has not yet been duplicated, because the study was designed to test a different hypothesis and therefore certain controls were not in place, and because the study was done on mice, not humans.

To be fair, none of those reasons suggest that there is not some correlation between cell phone radiation and better cognitive health in humans but the odds of that being proven remain very long, even with one study pointing in that direction.

This story, which I think has been reported with fair accuracy in the press (aside from the sensationalistic headlines) is quite indicative of how publishers sometimes fuel unreasonable expectations about scientific breakthroughs that are either too early or too unproven to warrant much excitement in terms of improved healthcare.

Contributed by: Michael Rafii, M.D., Ph.D - Director of the Memory Disorders Clinic at the University of California, San Diego. ______________________________________

High levels of the energy-regulating hormone leptin were associated with lower rates of Alzheimer's disease in a study appearing in The Journal of the American Medical Association. If confirmed, researchers say the findings could have important implications in the search for effective therapies to prevent and treat the disease.

Discovered in the mid-1990s, leptin is produced by fat cells and is believed to be critical for regulating hunger and weight. But there is growing evidence suggesting a role for the hormone in brain development and memory.

Leptin has been shown to reduce concentrations of Beta-amyloid, the major component of the deposits, or plaques, that occur in the brains of people with Alzheimer's disease.

In the new study, elderly people were followed for up to 15 years after blood leptin concentrations were measured. Over 12 years of follow-up, people with the lowest leptin levels were roughly four times more likely to develop Alzheimer's disease than people with the highest levels.

The study initially included 785 elderly people taking part in the ongoing Framingham Heart Study, which began recruiting patients in 1948. Blood leptin levels were measured between 1990 and 1994. Around eight years later, 198 of the participants who had not developed dementia underwent brain imaging with MRIs to assess brain aging. Those with the highest leptin levels at the beginning of the study had healthier brains with less evidence of aging. Higher early leptin concentrations were associated with lower rates of dementia years later. This association was seen even after they adjusted for the impact of midlife abdominal obesity, which has recently been identified as an early risk factor for Alzheimer's disease.

Future studies will be needed to understand the role of Leptin in AD, and whether leptin replacement could be a therapeutic approach.

This question is prone to a wide range of answers because physicians tend to address the question based on a strict, clinical definition of Alzheimer's disease whereas scientists adhere to a different definition. The rest of the world, including journalists, tends to consider the disease more generally. Let me explain.

Consider the intersection of four groups of people who might be involved in a "discussion" about Alzheimer's disease (such as this one recently posted at WebMD). There may be (1) the scientists who study the disease, (2) the physicians who treat the disease, (3) journalists and publishers who glean information from both the scientists and physicians before packaging it for delivery to the public, and (4) the lay-persons who consume all of that information.

There are common discrepancies between how each of these groups thinks about, and in fact define Alzheimer's disease. As such, one group's answer to the question (When Does Alzheimer's Disease Really Begin?) is frequently misinterpreted by a member of another group.

The scientists tend to think in terms of disease pathology. In their minds, as soon as some biological process initiates a cascade of other processes that will eventually lead to Alzheimer's lesions in the brain, then the disease has begun.

The physicians are bound by the duty of consistency to use the definition published and accepted by their peers. Since the clinical definition of Alzheimer's disease currently requires the presence of "dementia", then physicians peg the start of the disease at the point when the patient has accumulated so much brain damage that they can no longer care for themselves without human assistance.

The journalists and publishers are adept at gathering facts and packaging them into public messages. Being unaware of these diverse definitions, they often repeat "expert testimony" without realizing the nuances therein and without clarifying the context of their statements.

The public tends to think about the disease in terms of symptoms. That is, if one has memory loss or other cognitive difficulties, perhaps there is a disease at hand affecting their brain. If one has no symptoms then they are probably in good health. This perspective would consider the start of Alzheimer's to be at the onset of noticeable memory loss. That happens much later than the scientific perspective (biological change not yet manifest in symptoms) but much earlier than the clinical perspective (severe symptoms meeting the definition of dementia).

Here are two common scenarios, both of which lead to confusion.

A basic scientist might tell a journalist that Alzheimer's disease probably begins thirty years or so before the first symptoms appear. A healthy, lay-person reads the resulting article and worries needlessly about the prospect that they might already have the disease.

A prominent physician might tell a journalist that patients suffering from memory loss have mild cognitive impairment and may or may not convert to Alzheimer's disease. A lay-person who is clearly in cognitive decline and needs medical attention decides that they may not yet have reached the point where they should seek help.

So what's the answer to the question? It depends on who you ask. The underlying biological changes probably begin decades before early symptoms appear. From the onset of the subtlest symptoms, there is generally a 5-10 year period of mild cognitive impairment during which time an Alzheimer's patient maintains fairly high function and can live independently. This is also considered to be a period when treatment may be optimally beneficial so early detection of symptoms is important. Eventually, the symptoms worsen and the patient becomes demented with an average life expectancy of about 7 years from that point forward.

It really is amazing how much seemingly contradictory information is published about Alzheimer's and dementia each day when, in fact, most of the messages could be well aligned if more care were paid to definitions.